Damaged myelin generates abnormal rhythms in the sleeping brain
A new study reveals how the degeneration of the myelin sheath disrupts brain oscillations and rhythms during sleep, potentially providing non-invasive biomarkers for neurodegenerative diseases.
Damaged myelin generates abnormal rhythms in the sleeping brain
Scientists have identified how damage to the myelin sheath—the insulating layer surrounding nerve fibers—alters brain activity during sleep. The research, presented Friday, July 10, 2026, at the Federation of European Neuroscience Societies (FENS) Forum, suggests a biological link between the degeneration of this protective coating and the sleep disturbances frequently seen in neurodegenerative conditions.
Dr Mohit Dubey, a ZonMw Memorable Dementia Fellow at the Netherlands Institute for Neuroscience in Amsterdam, presented findings using electroencephalogram (EEG) recordings. In mouse models with damaged myelin and Alzheimer’s disease (AD), the EEG data revealed electrical spikes that appeared only while the mice were asleep. According to Dr Dubey, these spikes are similar to those observed in patients with AD or epilepsy.
The study focused on how the loss of myelin disrupts the efficiency of electrical signals within brain circuits. This degradation is a hallmark of several neurological diseases, including multiple sclerosis (MS) and AD.
"Sleep disturbances are extremely common in neurological diseases such as multiple sclerosis and Alzheimer’s disease, but the biological reasons for these problems remain poorly understood,"
Dr Mohit Dubey, via EurekAlert
To establish a broader connection, Dr Dubey and his team analyzed EEG recordings spanning several weeks and multiple nights in the mouse models and compared those results with EEG data from sleeping patients with MS. The team found that the abnormal electrical spikes in mice were tightly linked to sleep rhythms. Specifically, these spikes were associated with sleep spindles, which are bursts of brain activity occurring during the second stage of non-rapid eye movement (REM) sleep.
The research also identified a slowing of electrical rhythms that occur exclusively during REM sleep. This stage of sleep is characterized by dreaming and the replay of experiences from the day, utilizing rhythmic electrical patterns called oscillations to coordinate communication between neurons.
But when myelin degenerates, these oscillations become slower and disrupted. Dr Dubey stated that the electrical spikes observed during sleep are closely tied to the stability of brain circuits affected by AD and MS.
The implications of these findings extend to clinical diagnostics. Because sleep disturbances contribute to cognitive decline and fatigue in patients, understanding this biological link may allow for the development of non-invasive biomarkers. Dr Dubey suggested that sleep recordings could potentially detect early changes in brain circuit myelination before clinical symptoms appear, providing a tool for clinicians to monitor disease progression.
Professor Christina Dalla of the National and Kapodistrian University of Athens, who chairs the FENS Forum communication committee and was not part of the study, noted that the research showed a slowing of REM sleep oscillations in MS patients. She observed that this appears connected to disruptions in brain circuit connectivity and stability, similar to what was seen in mice with AD.
Currently, medical treatments exist to slow the immune system's attack on the myelin sheath in MS patients, but there are no treatments capable of repairing damaged myelin. The researchers believe that uncovering the biological basis of how myelin damage affects sleep could lead to the design of non-invasive strategies to repair myelin during sleep.
The study is characterized as a non-peer-reviewed observational study conducted in animals and people. While it successfully combines sleep neuroscience with the study of demyelinating circuits, the researchers acknowledged a limitation: the work was primarily conducted in mice. Further research is required to determine how these mechanisms translate to human disease.
Dr Dubey intends to focus his future research on the specific molecular and cellular mechanisms that link abnormal electrical activity, sleep rhythms, and myelin degeneration.
